ArticleNeuropharmacology2014
Repeated intermittent alcohol exposure during the third trimester-equivalent increases expression of the GABA(A) receptor δ subunit in cerebellar granule neurons and delays motor development in rats.
Article in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- Rat models of fetal alcohol spectrum disorders for studying the critical role of cerebellar damage: A scoping review.Alcohol, clinical & experimental research · 2025Article
- GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024Review
- Increased Voluntary Alcohol Consumption in Mice Lacking GABAFrontiers in behavioral neuroscience · 2022Article
- Impact of cisplatin administration on cerebellar cortical structure and locomotor activity of infantile and juvenile albino rats: the role of oxidative stress.Anatomical science international · 2022Article
- Ethanol effects on cerebellar myelination in a postnatal mouse model of fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.) · 2021Article
- Divergent and overlapping hippocampal and cerebellar transcriptome responses following developmental ethanol exposure during the secondary neurogenic period.Alcoholism, clinical and experimental research · 2021Article
- Characterization of motor function in mice developmentally exposed to ethanol using the Catwalk system: Comparison with the triple horizontal bar and rotarod tests.Behavioural brain research · 2021Article
- Increased Maternal Care Rescues Altered Reinstatement Responding Following Moderate Prenatal Alcohol Exposure.Alcoholism, clinical and experimental research · 2019Article
- Examining the effects of alcohol on GABAAlcohol (Fayetteville, N.Y.) · 2018Article
- An Overview of the Mechanisms of Abnormal GABAergic Interneuronal Cortical Migration Associated with Prenatal Ethanol Exposure.Neurochemical research · 2017Review
- Ethanol exposure during development reduces GABAergic/glycinergic neuron numbers and lobule volumes in the mouse cerebellar vermis.Neuroscience letters · 2016Article
- Third trimester-equivalent ethanol exposure causes micro-hemorrhages in the rat brain.Neuroscience · 2016Article
- Potentiation of Gamma Aminobutyric Acid Receptors (GABAAR) by Ethanol: How Are Inhibitory Receptors Affected?Frontiers in cellular neuroscience · 2016Review
- Sensitivity of GABAergic Tonic Currents to Acute Ethanol in Cerebellar Granule Neurons is Not Age- or δ Subunit-Dependent in Developing Rats.Alcoholism, clinical and experimental research · 2016Article
- Substance Use in the Perinatal Period.Current psychiatry reports · 2015Review
- Third trimester-equivalent ethanol exposure increases anxiety-like behavior and glutamatergic transmission in the basolateral amygdala.Pharmacology, biochemistry, and behavior · 2015Article
- Mini-Review: Effects of Ethanol on GABAA Receptor-Mediated Neurotransmission in the Cerebellar Cortex--Recent Advances.Cerebellum (London, England) · 2015Review
- Impaired arousal in rat pups with prenatal alcohol exposure is modulated by GABAergic mechanisms.Physiological reports · 2015Article
- Effect of repeated alcohol exposure during the third trimester-equivalent on messenger RNA levels for interleukin-1β, chemokine (C-C motif) ligand 2, and interleukin 10 in the developing rat brain after injection of lipopolysaccharide.Alcohol (Fayetteville, N.Y.) · 2014Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Exposure to ethanol (EtOH) during fetal development can lead to long-lasting alterations, including deficits in fine motor skills and motor learning. Studies suggest that these are, in part, a consequence of cerebellar damage. Cerebellar granule neurons (CGNs) are the gateway of information into the cerebellar cortex. Functionally, CGNs are heavily regulated by phasic and tonic GABAergic inhibition from Golgi cell interneurons; however, the effect of EtOH exposure on the development of GABAergic transmission in immature CGNs has not been investigated. To model EtOH exposure during the 3rd trimester-equivalent of human pregnancy, neonatal pups were exposed intermittently to high levels of vaporized EtOH from postnatal day (P) 2 to P12. This exposure gradually increased pup serum EtOH concentrations (SECs) to ∼60 mM (∼0.28 g/dl) during the 4 h of exposure. EtOH levels gradually decreased to baseline 8 h after the end of exposure. Surprisingly, basal tonic and phasic GABAergic currents in CGNs were not significantly affected by postnatal alcohol exposure (PAE). However, PAE increased δ subunit expression at P28 as detected by immunohistochemical and western blot analyses. Also, electrophysiological studies with an agonist that is highly selective for δ-containing GABA(A) receptors, 4,5,6,7-tetrahydroisoxazolo[4,5-c]pyridine-3-ol (THIP), showed an increase in THIP-induced tonic current. Behavioral studies of PAE rats did not reveal any deficits in motor coordination, except for a delay in the acquisition of the mid-air righting reflex that was apparent at P15 to P18. These findings demonstrate that repeated intermittent exposure to high levels of EtOH during the equivalent of the last trimester of human pregnancy has significant but relatively subtle effects on motor coordination and GABAergic transmission in CGNs in rats.
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